DEEP VEIN THROMBOSIS DR. PRIYADARSHAN KONAR PGT 2 ND YR DEPT OF GENERAL SURGERY
DEFINITION Deep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg.
IT IS LIKE ICEBERG DISEASE Symptomatic deep vein thrombosis is "tip of the iceberg"
VIRCHOW TRIAD Rudolf Ludwig Carl Virchow (1821-1902) Prof Of Pathology, Germany, Berlin Described three factors that are thought to contribute to thrombosis - Venous stasis Hypercoagulable state Endothelial damage
VENOUS STASIS Prolonged bed rest (4 days or more) A cast on the leg Limb paralysis from stroke Spinal cord injury extended travel in a vehicle
HYPERCOAGULABILITY Surgery and trauma - 40% of all thrombo embolic disease Malignancy increased estrogen Inherited disorders of coagulation - Deficiencies of protein-S, protein-C, anti-thrombin III . Acquired disorders of coagulation- Nephrotic syndrome, Anti-phospholipid antibodies
ENDOTHELIAL INJURY Trauma Surgery Invasive procedure Iatrogenic causes – central venous catheters Subclavian Internal jugular lines These lines cause of upper extremity DVT.
HYPERCOAGULABLE STATE OF MALIGNANCY Up to 15% of cancer patients presents with VTE VTE is not equally common in all types of cancer . Â The highest incidence is found in mucin- producing adenocarcinomas, pancreas and gastrointestinal tract, lung cancer, and ovarian cancer.
PATHOLOGY OF DVT A thrombus develops in soleal veins initially as a platelet aggregate. Fibrin and red cells form a mesh until lumen of vein wall occludes. Coralline thrombus then progresses as a propagated loose red fibrin clot containing many red cells. Extend up to next large venous branch Possible for clot to break off Pulmonary embolism
PRESENTATION AND PHYSICAL EXAMINATION Calf pain or tenderness, or both Swelling with pitting edema Increased skin temperature and fever Superficial venous dilatation Cyanosis can occur with severe obstruction
Less frequent manifestations of venous thrombosis include :- Phlegmasia alba dolens , Phlegmasia cerulea dolens , and Venous gangrene. These are clinical spectrum of the same disorder.
CLINICAL FEATURES Sudden severe pain , Swelling, Cyanosis Edema of the affected limb. There is a high risk of massive pulmonary embolism, even under anticoagulation. Foot gangrene may also occur. An underlying malignancy is found in 50% of cases.
CLINICAL EXAMINATION Palpate distal pulses and evaluate capillary refill to assess limb perfusion. Move and palpate all joints to detect acute arthritis or other joint pathology. Neurologic evaluation may detect nerve root irritation; sensory, motor, and reflex deficits should be noted
Homans Sign : Pain In The Posterior Calf Or Knee With Forced Dorsiflexion Of The Foot.
Moses sign Gentle squeezing of the lower part of the calf from side to side. Neuhofs sign Thickening and deep tenderness elicited while palpating deep in calf muscles. Lintons sign After applying torniquet at saphenofemoral junction patient made to walk , then limb is elevated in supine posation prominent superficial veins will be observed.
WELLS CLINICAL PREDICTION GUIDE Its a pre-test probability score Helps in:- early risk stratification and appropriate use of laboratory tests and imaging modalities. wells criteria is an additional tool to diagnosis rather than being a stand-alone test.
Interpretation High probability: ≥ 3 (Prevalence of DVT - 53%) Moderate probability: 1-2 (Prevalence of DVT - 17 %) Low probability: ≤ 0 (Prevalence of DVT - 5%)
DIAGNOSTIC STUDIES Clinical examination alone is able to confirm only 20-30% of cases of DVT Blood Tests The D-dimer Imaging Studies
D-DIMER It specific degradation product of cross-linked fibrin. Because concurrent production and breakdown of clot characterize thrombosis, patients with thromboembolic disease have elevated levels of D-dimer. Three major approaches for measuring D-dimer ELISA  latex agglutination  blood agglutination test
Various kits have a 93-95% sensitivity and about 50% specificity in the diagnosis of thrombotic disease. False-positive D-dimers occur in patients with :- recent (within 10 days) surgery or trauma, recent myocardial infarction or stroke, acute infection, disseminated intravascular coagulation, pregnancy or recent delivery, active collagen vascular disease, or metastatic cancer
ALGORITHM FOR DIAGNOSTIC IMAGING
Imaging studies INVASIVE NONINVASIVE Â ultrasound, Â plethysmography, Â MRI techniques venography , radiolabeled fibrinogen
VENOGRAM : POPLITEAL VEIN THROMBOSIS
VENOGRAPHY It detects thrombi in both calf and thigh It can conclude and exclude the diagnosis of DVT when other objective testings are not conclusive. ADVANTAGES It is useful if the patient has a high clinical probability of thrombosis and a negative ultrasound. It is also valuable in symptomatic patients with a history of prior thrombosis in whom the ultrasound is non-diagnostic .
DISADVANTAGE It can primary cause of DVT in 3% of patients who undergo this diagnostic procedure. An invasive and expensive. Although Venography was once considered the gold standard for diagnosis of DVT, today it is more commonly used in research environments and less frequently utilized in clinical practice.
NUCLEAR MEDICINE STUDIES Because the radioactive isotope incorporates into a growing thrombus, this test can distinguish new clot from an old clot. Nuclear medicine studies done with I 125 -labeled fibrinogen. More commonly used in research.
PLETHYSMOGRAPHY Plethysmography measures change in lower extremity volume in response to certain stimuli.
IMPEDANCE PLETHYSMOGRAPHY Principle - Blood volume changes in the leg lead to changes in electrical resistance. Venous return in the lower extremity is occluded by inflation of a thigh cuff, and then the cuff is released, resulting in a decrease in calf blood volume. Any obstruction of the proximal veins diminishes the volume change, which is detected by measuring changes in electrical resistance (impedance) over the calf.
ULTRASONOGRAPHY Color-flow duplex scanning is the imaging test of choice for patients with suspected DVT Inexpensive, Noninvasive, Widely available Ultrasound can also distinguish other causes of leg swelling, such as tumor, popliteal cyst, abscess, aneurysm, or hematoma.
MAGNETIC RESONANCE IMAGING It detects leg, pelvis, and pulmonary thrombi and is 97% sensitive and 95% specific for DVT. It distinguishes a mature from an immature clot. MRI is safe in all stages of pregnancy. Test may not be appropriate for patients with pacemakers or other metallic implants, it can be an effective diagnostic option for some patients.
MANAGEMENT Using the pretest probability score calculated from the Wells Clinical Prediction rule, patients are stratified into 3 risk groups—high, moderate, or low. The results from duplex ultrasound are incorporated as follows: If the patient is high or moderate risk and the duplex ultrasound study is positive treat for DVT.
If the duplex study is negative and the patient is low risk , DVT has been ruled out. When discordance exists between the pretest probability and the duplex study result, further evaluation is required. If the patient is high risk but the ultrasound study was negative, the patient still has a significant probability of DVT
a venogram to rule out a calf vein DVT surveillance with repeat clinical evaluation and ultrasound in 1 week. results of a D-dimer assay to guide management If the patient is low risk but the ultrasound study is positive, some authors recommend a second confirmatory study such as a venogram before treating for DVT
The primary objectives of the treatment of DVT are to :- prevent pulmonary embolism, reduce morbidity, and prevent or minimize the risk of developing the postphlebitic syndrome .
GENERAL THERAPEUTIC MEASURES : Bed rest . Encourage the patient to perform gentle foot & leg exercises every hour. Increase fluid intake upto 2 l/day unless contraindicated. Avoid deep palpation .
SPECIFIC TREATMENT : Anticoagulation Thrombolytic therapy for DVT Surgery for DVT Filters for DVT Compression stockings
Initial treatment of DVT is with low- molecular-weight heparin or unfractionated heparin for at least 5 days, followed by warfarin (target INR, 2.0–3.0) for at least 3 months.
Heparin: Mechanism of Action Accelerates antithrombin III activity
DOSE IV bolus dose of 5,000 to 10,000 units followed by an infusion of 1,000 units per hour. Other method of initiating therapy is to begin with Loading dose of 50-100 units/kg of heparin followed by a constant infusion of 15-25 units/kg/hr.
LOW MOLECULAR WEIGHT HEPARIN Selectively inhibit factor Xa . Superior bioavailability Superior or equivalent safety and efficacy Subcutaneous once- or twice-daily dosing No laboratory monitoring Less phlebotomy (no monitoring/no intravenous line) Less thrombocytopenia
The optimal regimen for the treatment of DVT is anticoagulation with heparin or an LMWH followed by full anticoagulation with oral warfarin for 3-6 months Warfarin therapy is overlapped with heparin for 4-5 days until the INR is therapeutically elevated to between 2-3.
WARFARIN Interferes with hepatic synthesis of vitamin K- dependent coagulation factors Dose must be individualized and adjusted to maintain INR between 2-3 Oral dose of 2-10 mg/d caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis
WARFARIN—MECHANISM OF ACTION
SURGERY FOR DVT Indications when anticoagulant therapy is ineffective unsafe, contraindicated. The major surgical procedures for DVT are clot removal and partial interruption of the inferior vena cava to prevent pulmonary embolism.
These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated.
THIS PATIENT UNDERWENT A THROMBECTOMY. THE THROMBUS HAS BEEN LAID OVER THE APPROXIMATE LOCATION IN THE LEG VEINS WHERE IT DEVELOPED.
Filters for dvt T his tiny umbrella-like device is inserted into the vein to catch blood clots and stop them moving up into the lungs, while allowing blood flow to continue. It is inserted in the vena cava.